Annual Bluegrass (Poa annua) is a monocot weed in the Poaceae family. In Victoria this weed first evolved resistance to Group C1/5 herbicides in 2017 and infests Golf courses. Group C1/5 herbicides are known as Photosystem II inhibitors (Inhibition of photosynthesis at photosystem II). Research has shown that these particular biotypes are resistant to simazine and they may be cross-resistant to other Group C1/5 herbicides.

The 'Group' letters/numbers that you see throughout this web site refer to the classification of herbicides by their site of action. To see a full list of herbicides and HRAC herbicide classifications click here.

Greenhouse trials comparing a known susceptible Annual Bluegrass biotype with this Annual Bluegrass biotype have been used to confirm resistance. For further information on the tests conducted please contact the local weed scientists that provided this information.

Genetics

Genetic studies on Group C1/5 resistant Annual Bluegrass have not been reported to the site. There may be a note below or an article discussing the genetics of this biotype in the Fact Sheets and Other Literature

Mechanism of Resistance

The mechanism of resistance for this biotype is either unknown or has not been entered in the database. If you know anything about the mechanism of resistance for this biotype then please update the database.

Relative Fitness

Triazine resistant weeds often exhibit a lower relative fitness when compared to susceptible biotypes. The most common mutation conferring triazine resistance (Ser 264 to Gly mutation of the psbA gene) also causes a reduction in CO2 fixation, quantum yield, and seed and biomass production. There is no record in this database referring specifically to fitness studies on Group C1/5 resistant Annual Bluegrass from Victoria.

The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in Victoria have been instrumental in providing you this information. Particular thanks is given to Peter Boutsalis for providing detailed information.

Resistance to acetolactate synthase (ALS) and photosystem II inhibiting herbicides was confirmed in a population of allotetraploid annual bluegrass (Poa annua L.; POAAN-R3) selected from golf course turf in Tennessee. Genetic sequencing revealed that seven of eight POAAN-R3 plants had a point mutation in the psbA gene resulting in a known Ser-264-Gly substitution on the D1 protein. Whole plant testing confirmed that this substitution conferred resistance to simazine in POAAN-R3. Two homeologous forms of the ALS gene (ALSa and ALSb) were detected and expressed in all POAAN-R3 plants sequenced. The seven plants possessing the Ser-264-Gly mutation conferring resistance to simazine also had a homozygous Ala-205-Phe substitution on ALSb, caused by two nucleic acid substitutions in one codon. In vitro ALS activity assays with recombinant protein and whole plant testing confirmed that this Ala-205-Phe substitution conferred resistance to imidazolinone, sulfonylurea, triazolopyrimidines, sulfonylamino-carbonyl- triazolinones, and pyrimidinyl (thio) benzoate herbicides. This is the first report of Ala-205-Phe mutation conferring wide spectrum resistance to ALS inhibiting herbicides..

Prodiamine is a mitotic inhibiting herbicide regularly used to control annual bluegrass PRE. A population of annual bluegrass not controlled by prodiamine at 1,120 g a.i. ha-1 was identified on a golf course in Alcoa, TN, in 2012. A whole-plant hydroponics bioassay was used to screen this biotype for prodiamine resistance (PR) compared with a known susceptible population (SS). Multitiller (i.e., >4 tillers) PR and SS annual bluegrass plants were established in hydroponic culture and exposed to 0, 0.001, 0.01, 0.10, 1.0, and 10.0 mM prodiamine. Exposure to prodiamine at 0.001 mM reduced root growth of the SS biotype to 26% of the nontreated check (i.e., 0 mM prodiamine) but had no effect on the PR biotype. When exposed to 10 mM prodiamine, root growth of the PR biotype was reduced to 24% of the nontreated check compared with 9% for the SS biotype. I50 values for the PR and SS biotypes were 0.04 and 2.8×10-6 mM prodiamine, respectively. The PR biotype measured lower in plant height and leaf width than the SS population. In field trials, prodiamine at 560, 840, 1,120, and 1,400 g ha-1 only controlled the PR biotype 0 to 22%. PRE applications of the cellulose biosynthesis inhibitor indaziflam at 35, 52.5, and 70 g a.i. ha-1 controlled this PR biotype 70 to 97%. This marks the second instance of annual bluegrass developing resistance to prodiamine in Tennessee during the past 5 yr. Future research should evaluate indaziflam efficacy for control of other prodiamine-resistant biotypes of annual bluegrass as well as annual bluegrass biotypes resistant to herbicidal inhibitors of 5-enolpyruvylshikimic acid-3-phosphate synthase, acetolactate synthase, and photosystem II..

Herbicide resistance or tolerance in weeds mediated by cytochrome P450 monooxygenase is a considerable problem. However, cytochrome P450 mediated resistance or tolerance in weeds was less studied. Thus, in this work, the role of the cytochrome P450 monooxygenase in the different responses of Poa annua and Alopecurus aequalis to fenoxaprop-P-ethyl was studied. We found that the effect of fenoxaprop-P-ethyl could be synergized by piperonyl butoxide (PBO) in P. annua, but not by malathion. After being treated with fenoxaprop-P-ethyl (containing mefenpyr-diethyl), the contents of cytochrome P450 and cytochrome b5 in P. annua increased significantly compared to plants treated with mefenpyr-diethyl only or untreated plants. However, the increase was less in A. aequalis, which was susceptible to fenoxaprop-P-ethyl. The activities of ρ-nitroanisole O-demethylase (PNOD), ethoxyresorufin O-deethylase (EROD), ethoxycoumarin oxidase (ECOD) and NADPH-dependent cytochrome P450 reductase mediated by cytochrome P450 monooxygenase increased in P. annua after treatment with fenoxaprop-P-ethyl, especially the activities of ECOD and cytochrome P450 reductase. Besides this, cytochrome P450 monooxygenase activity toward fenoxaprop-P-ethyl in P. annua increased significantly compared to untreated or treated with mefenpyr-diethyl plants and treated or untreated A. aequalis. Cytochrome P450 monooxygenase may play an important role in the different responses to fenoxaprop-P-ethyl in P. annua and A. aequalis..

Evolved herbicide resistance (EHR) is an important agronomic problem and consequently a food security problem, as it jeopardizes herbicide effectiveness and increases the difficulty and cost of weed management. EHR in weeds was first reported in 1970 and the number of cases has accelerated dramatically over the last two decades. Despite 40 years of research on EHR, why some weeds evolve resistance and others do not is poorly understood. Here we ask whether weed species that have EHR are different from weeds in general. Comparing taxonomic and life history traits of weeds with EHR to a control group ("the world's worst weeds"), we found weeds with EHR significantly over-represented in certain plant families and having certain life history biases. In particular, resistance is overrepresented in Amaranthaceae, Brassicaceae and Poaceae relative to all weeds, and annuality is ca. 1.5 times as frequent in weeds with EHR as in the control group. Also, for perennial EHR weeds, vegetative reproduction is only 60% as frequent as in the control group. We found the same trends for subsets of weeds with EHR to acetolactate synthase (ALS), photosystem II (PSII), and 5-enolpyruvylshikimate-3-phosphate (EPSP) synthase-inhibitor herbicides and with multiple resistance. As herbicide resistant crops (transgenic or not) are increasingly deployed in developing countries, the problems of EHR could increase in those countries as it has in the USA if the selecting herbicides are heavily applied and appropriate management strategies are not employed. Given our analysis, we make some predictions about additional species that might evolve resistance..

Annual bluegrass is the most problematic winter annual weed in managed turfgrass. Acetolactate synthase (ALS)-inhibiting herbicides are effective for annual bluegrass control, but reliance on this mode of action can select for herbicide-resistant biotypes. Two annual bluegrass biotypes not controlled with ALS-inhibiting herbicides were reported at golf courses in South Carolina and Georgia. Research was initiated at Clemson University to verify the level of resistance of these biotypes to ALS inhibitors. Two ALS-susceptible (S) and suspected resistant (SCr, GAr) annual bluegrass biotypes were established in a greenhouse. Dose-response experiments were conducted on mature annual bluegrass plants using trifloxysulfuron, foramsulfuron, and bispyribac-sodium, all ALS-inhibiting herbicides. Additionally, a rapid diagnostic ALS activity assay was optimized and conducted using the same herbicides. For dose-response experiments, the rate of herbicide that reduced shoot biomass 50% (I50) values for the S biotypes were 13.6 g ai ha-1 for trifloxysulfuron, 7.0 g ai ha-1 for foramsulfuron, and 38.3 g ai ha-1 for bispyribac-sodium. Fifty percent shoot biomass reduction was not observed in either the SCr or GAr biotypes at eight times the labeled field rate of all ALS-inhibiting herbicides tested. For in vivo tests of ALS activity, the SCr biotype yielded I50 (concentration of herbicide that reduced ALS activity 50%) values 3,650, 3,290, and 13 times the S biotypes following treatment with trifloxysulfuron, foramsulfuron, and bispyribac-sodium, respectively. Similarly, I50 values for the GAr biotype were 316, 140, and 64 times greater than the S biotypes following the same herbicide treatments. This research indicates high levels of annual bluegrass resistance to multiple ALS-inhibiting herbicides in South Carolina and Georgia. Future research should focus on the mechanisms of ALS resistance in these annual bluegrass biotypes as well as alternative options for control not targeting the ALS enzyme..